Studies show that adverse conditions during early life can increase vulnerability to mood disorders later in life. There is also much evidence linking mood disorders to alterations in the inflammatory system including the presence of elevated levels of pro-inflammatory cytokines, together with other mediators of inflammation. Levels of environmental adversity in the early developmental period is able to shape maturation of stress-regulating and immune pathways leading to long-lasting alterations in stress responsivity and immune functioning during adulthood. Current research is addressing the molecular mechanisms underlying this programming, by which exposure to early life adversity represents a vulnerability factor for the development of psychiatric disorders that act through the modulation of inflammatory responses. In this article, we focus on evidence suggesting that epigenetic changes, established early in life, drive connections between long-term outcomes, specifically implicated in long-term perturbations in HPA axis and glucocorticoid regulation and immune system functioning
